PubMed | Australian National University, Doherty Institute, Mycobacterium Reference Laboratory and University of MelbourneType: Journal Article | Journal: The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease | Year: 2016

Victoria, Australia.To measure the level of Mycobacterium tuberculosis transmission in Victoria.Retrospective analysis of mycobacterial interspersed repetitive unit-variable number of tandem repeats (MIRU-VNTR) typing profiles from all first M. tuberculosis complex (MTC) isolates obtained from patients residing in Victoria from 2003 to 2010 was performed. State TB reference laboratory records were matched with Department of Health notification records to obtain further laboratory, demographic, contact investigation, clinical and treatment data. These data were used to assign patients to one of four categories: 1) no epidemiological link, 2) possible link, 3) likely transmission event and 4) laboratory contamination.A total of 2377 MTC isolates were genotyped using 15-locus MIRU-VNTR. Of the 2298 M. tuberculosis isolates, 1029 (44.8%) had unique genotypic profiles and were considered epidemiologically unrelated, while 1269 (55.2%) isolates shared a profile with one or more other strains, defined as a genotypic cluster. Systematic investigation of all 268 genotypic clusters, including 24-locus MIRU-VNTR on selected isolates, led to a further 862 patients being classified as unrelated, bringing the total number of patients with no epidemiological links to 1891 (82.3%). Of the remaining patients, 294 (12.8%) were classified as having possible epidemiological links, 96 (4.2%) were classified as having known epidemiological links representing likely transmission events and 17 (0.7%) as the result of laboratory cross-contamination.There is considerable genotypic diversity among Victorian MTC isolates, and the level of transmission is low.

Chronic infection with hepatitis B virus (HBV) greatly increases the risk for liver cirrhosis and hepatocellular carcinoma (HCC). HBV isolates worldwide can be divided into ten genotypes. Moreover, the immune clearance phase selects for mutations in different parts of the viral genome. The outcome of HBV infection is shaped by the complex interplay of the mode of transmission, host genetic factors, viral genotype and adaptive mutations, as well as environmental factors. Core promoter mutations and mutations abolishing hepatitis B e antigen (HBeAg) expression have been implicated in acute liver failure, while genotypes B, C, subgenotype A1, core promoter mutations, preS deletions, C-terminal truncation of envelope proteins, and spliced pregenomic RNA are associated with HCC development. Our efforts to treat and prevent HBV infection are hampered by the emergence of drug resistant mutants and vaccine escape mutants. This paper provides an overview of the HBV life cycle, followed by review of HBV genotypes and mutants in terms of their biological properties and clinical significance.